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Adult Brain Neurogenesis and Psychiatry - a Novel Theory of Depression - Article Example

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The article “Adult Brain Neurogenesis and Psychiatry - a Novel Theory of Depression” offers exactly what it promises, a new theory regarding the causes and possible effective cures of adult clinical depression as it is linked with the process of the birth of new neurons in the human brain…
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Adult Brain Neurogenesis and Psychiatry - a Novel Theory of Depression
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Article: Adult Brain Neurogenesis and Psychiatry The article en d “Adult Brain Neurogenesis and Psychiatry: A Novel Theory of Depression” offers exactly what it promises, a new theory regarding the causes and possible effective cures of adult clinical depression as it is linked with the process of neurogenesis, or the birth of new neurons in the human brain. The article presents a detailed literature review in which the various elements of their theory are discussed including a description of what neurogenesis is, how it may affect general behavior and how behavior may be affected by it. After making these connections, the authors discuss studies in which it was determined that interruption in neural creation may be one of the major factors in precipitating depression based upon how they believe the process works. Neurogenesis is introduced as the process of making new neurons in the brain, something that occurs to a great degree during development even into childhood, but was thought to cease as the individual moves into their adult years. The authors indicate new science that has revealed neurogenesis does occur in the adult brain, however, particularly in two specific regions, one of which is the hippocampus, which has also been linked to a number of mental disorders. With this revelation into the workings of the brain, the authors suggest there could be a significant implication for possible treatment options not only for psychoses of the brain, but also for damage reparation following trauma or illness. As an example, they present their hypothesis regarding the connection between neurogenesis and depression. A provided review of the terminology to be used is helpful not only by introducing the terms and what is meant by them, but also in illustrating how these cellular structures relate to the concept of information processing. Once it is established that new neurons are being produced, the authors discuss those elements that seem to lead to increased or decreased neuron production in terms of behavior (exercise and learning to increase; seizure, stress or trauma to decrease), chemicals or drugs, particularly glucocorticoids, and genetics in which none of these causes were able to exclude the others. In other words, stressed environment coupled with the right chemicals could produce the same amount or greater number of new neurons as an enriched environment and poor genes depending upon the balance struck between the inducing and prohibiting influences. The study proposes that, because stress is known to effect the development of cells in the hippocampus and it is known to induce depression, “it is reasonable to propose that a stress-induced decrease in neurogenesis may be an important factor in precipitating episodes of depression” (264) and thus, increases in neurogenesis may be helpful in recovering from depression. The literature review provides evidence that stress can inhibit neurogenesis in numerous mammals and it is expected to have the same effect in humans. For example, the study cites a trial in which cell proliferation was suppressed when adult rats were exposed to the scent of one of their natural predators (265). They also cite other studies in which it was found that stress could lead to suppression of cell generation in other areas of the body and could even cause sell death. The link between clinical depression with the hippocampus is proved with similar citation of studies and characteristics of various illnesses, such as Cushing’s Disease and Temporal Lobe Epilepsy. Under both of these conditions, large portions of the hippocampus are damaged and depression occurs in these patients at a far higher incidence rate than the general population. A link has also been made to the effects of serotonin on neurogenesis as it has been revealed through drug therapy. According to the authors, there is a hypothesis that serotonin increases neurogenesis through some action taken at the 5-HT receptor, of which the hippocampus has an unusually dense concentration. The authors admit other probable causes of depression as being equally valid. “… increases and decreases in serotonin neurotransmission, besides affecting hippocampal neurogenesis, may exert additional direct effects on the brain stem, subcortical sites, and in the cortex. All of these changes, acting in concert, give rise to the complex syndrome of depression” (266). The authors continue to emphasize the role of other possible solutions, such as the findings that exercise can increase the production of neurons within the hippocampus throughout the discussion. Rather than positioning their hypothesis against other theories that have been proposed, the authors suggest that their study helps to explain the process by which these other theoreticized processes might function. For example, the theory successfully and simply provides an answer for the ‘therapeutic lag’ that occurs before a patient begins feeling better after starting anti-depressant medication. The authors provide numerous suggestions for future research in the field of neurogenesis. These include determining why and how this process occurs within the specific areas of the adult brain in a normal case so that predictions can be made regarding what is likely to happen when disruptions occur. It is suggested that the discovery of new neuron production in the adult brain must necessarily change our perceptions of how the brain works, and thus may begin to introduce new understandings of various conditions such as depression. In addition, the authors suggest that the therapeutic benefits of neurogenesis could be astounding as these cells can be withdrawn from the adult brain, cultured, differentiated and expanded and transplanted into damaged brain regions for a more complete recovery or induced to proliferate within the body through such measures as drug therapy or physical activity. Multiple Choice Questions 1. What is a progenitor cell? a. The most primitive cell structure currently known b. Cells that can divide indefinitely c. The first type of differentiated cell d. Cells that can divide for a limited number of times 2. According to the study, what are two conditions that help to link damage to the hippocampus with depression? a. Downs Syndrome and Heart Disease b. Temporal Lobe Epilepsy and Alzheimer’s c. Cushing’s Disease and Temporal Lobe Epilepsy d. Alzheimer’s and Cushing’s Disease Essay Question Based on the information provided in the article, what is hypothesized to be the process through which stress causes depression and how the process can be reversed? According to the hypothesis in the article, stress is thought to cause depression by interrupting or halting the production of new neurons within the hippocampus which play a role, still unknown, in the proper function of the brain’s memory and information processing functions. The theory is based on newly discovered evidence that the adult brain does produce new neural cells in the hippocampus and at least one other area of the brain. Although the function of these cells is not precisely known, it is thought that they play a significant role in information processing and memory storage. It is important to have this knowledge before investigating the process by which stress is thought cause depression. Based on the information in the article, stress begins to interrupt the production of new cells throughout various systems, including within the hippocampus. At the same time, it has been shown that those individuals who experience long-term depression have a smaller hippocampus and that the hippocampus shrinks when it is not busy working at producing new cells. Thus, a link is established where stress prevents the healthy functioning of the hippocampus which somehow brings on bouts of depression. If this mysterious process were simply the need to re-start the hippocampus, therapeutic interventions such as drug therapy should produce nearly immediate results in mood in much the same way that re-starting the heart produces immediate results in blood circulation. However, there has always been a ‘therapeutic lag’ in which patients have had to remain on anti-depressant medication for as long as two months before effects begin to be felt. This ‘therapeutic lag’ suggests some other process must be at work. The theory offered is that because the hippocampus has numerous 5-HT receptors, which are thought to help the process by which serotonin induces neurogenesis, and that it is one of the only places in the brain where new cells are continuously generated and that it would take approximately one to two months for these new cells to develop sufficiently to function, the presence of these cells must play some role in the development of depression. Thus, increasing the production of new cells could be an effective treatment, and perhaps is currently an effective treatment, for clinical depression. Works Cited Jacobs, BL; van Praag, H. & Gage, FH. “Adult Brain Neurogenesis and Psychiatry: A Novel Theory of Depression.” Molecular Psychology. Vol. 5, (2000), pp. 262-269. Read More
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